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1

Serum levels of cytokines in alcoholic liver cirrhosis and pancreatitis

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Szuster-Ciesielska A., Daniluk J., Kandefer-Szerszen M.
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vol. 48
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issue 4
301-307
EN
Although altered cytokine homeostasis has been implicated in the pathogenesis of both alcoholic liver and pancreas diseases, the serum cytokine pattern characteristic of concomitant alcoholic liver cirrhosis and pancreatitis has not been examined. In this paper we examine the serum levels of proinflammatory cytokines, such as IL-6, IL-8, TNF-alpha, and also antiinflammatory ones, such as IL-10 and TGF-beta, in 22 patients with alcoholic liver cirrhosis and 28 patients with chronic pancreatitis and compare them with those detected in the sera of 14 patients with concomitant alcoholic cirrhosis and pancreatitis. All patients were heavy alcohol drinkers, consuming more than 70 g of pure alcohol per day for at least 5 years. The control group consisted of 33 age- and sex-matched healthy subjects receiving an annual health examination. They were not addicted to alcohol and confirmed to be free of major cardiopulmonary, gastrointestinal and hepatobiliary-pancreatic diseases. The results indicated that the cytokine pattern in the sera of patients with concomitant liver cirrhosis and pancreatitis was characterized by increased levels of two proinflammatory cytokines: TNF-alpha, the concentration of which seemed to be influenced by both liver and pancreas injury, and IL-6, which seemed to be rather connected with pancreas injury. Increased levels of IL-8, which were detected in the sera of patients with cirrhosis, pancreatitis and concomitant cirrhosis and pancreatitis, were rather connected with exacerbation of the disease processes which occurred only in some of the patients. No significant changes in the levels of IL-10 or TGF-beta were detected in the sera of patients with chronic pancreatitis and concomitant cirrhosis and pancreatitis, while in patients with cirrhosis significantly decreased levels of IL-10 were found. A significant imbalance between proinflammatory/antiinflammatory signals was especially characteristic of alcoholic cirrhosis and concomitant cirrhosis with pancreatitis.
2

Alcohol-related cirrhosis with pancreatitis. The role of oxidative stress in the progression of the disease

100%
Szuster-Ciesielska A., Daniluk J., Kandefer-Szerszen M.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
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issue 2
139-146
EN
To assess the level of oxidative stress, measured as prooxidant-antioxidant imbalance in the blood of patients with alcohol-related injury of the liver and pancreas, we determined superoxide ion (O2?-) production by neutrophils isolated from the peripheral blood of 3 groups of patients. Patients with compensated alcoholic liver cirrhosis (n=16), with alcoholic chronic pancreatitis (n=20), and with concomitant cirrhosis and pancreatitis (n=10) were included in this study. All patients had consumed at least 70 g of pure alcohol per day over 5 years. They had not abstained before admission to hospital. The control group consisted of 16 healthy non-alcohol-abusive subjects. As antioxidative enzymes (AOE) present in sera play a very important role in the regulation of plasma ROS levels and in the protection of plasma compounds against ROS action, we also examined serum activity of CAT, SOD (total activity) and GPx serum concentration. Neutrophils of patients with concomitant alcoholic liver cirrhosis and pancreatitis exhibited, similarly to the neutrophils of patients with chronic alcoholic pancreatitis, an enhanced ability to produce superoxide anions in vitro. In contrast, neutrophils of patients with alcoholic liver cirrhosis exhibited a defect in resting and PMA-induced superoxide anion production. The AOE activity in the sera of patients was also significantly changed. Total SOD activity was enhanced in all groups of patients with alcoholic liver cirrhosis, chronic pancreatitis and with concomitant injury of both organs. CAT activity was only increased in the sera of patients with liver cirrhosis or pancreatitis, but not in the patients with concomitant cirrhosis and pancreatitis. GPx concentration was only diminished in the patients with chronic pancreatitis. It seems likely that oxidative stress, defined as the imbalance between prooxidant and antioxidant activity, is highest in the blood of patients with chronic pancreatitis and, especially, in patients with concomitant liver cirrhosis and pancreatitis.
3

Neuroleptics modulate cytokine and reactive oxygen species production in blood leukocytes of healthy volunteers

88%
Szuster-Ciesielska A., Slotwinska M., Stachura A., Marmurowska-Michalowska H., Kandefer-Szerszen M.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 1
59-67
EN
There have been several reports indicating that schizophrenia is related to the activation of the inflammatory response system (IRS),characterized by increased serum concentrations of several cytokines,and that antipsychotic drugs may have immunosuppressive or immunoreg- ulatory effects.The aim of the present study was to examine the effects of neuroleptics on cytokine and reactive oxygen species production in vitro,in blood leukocytes. We studied the effect of haloperidol,chlorpromazine and clozapine on the unstimulated and stimulated (phytohemagglutinin+lipopolysaccharide ?PHA+LPS)production of some cytokines which are known to be mainly products of T lymphocytes and monocytes (IL-2, lymphotoxin,IFN-? ,IL-12,IL-4,IL-10 and TGF-? )in peripheral blood mononuclear cells (PBMC)of healthy subjects.We also compared the effect of neuroleptics on superoxide anion and hydrogen peroxide production in blood neutrophils. All three antipsychotic drugs significantly increased PHA+LPS-stimulated production of anti-inflammatory cytokines such as IL-10 and TGF-? as well as unstimulated production of IL-10,but they did not influence IL-12 production.In the same in vitroconditions they inhibited PHA+LPS-stimulated production of IL-2 and lymphotoxin.IL-4 production was inhibited by haloperidol and chlorpromazine,but not by clozapine.IFN-? production was inhibited by haloperidol and chlorpromazine,but stimulated by clozapine.All neuroleptics examined at a high (100 muM)concentration,but not at a 1 muM concentration,significantly inhibited superoxide anion production by phorbol ester (PMA)-stimulated neutrophils in vitro. The results indicate that in vitro typical antipsychotic drugs, such as haloperidol and chlor- promazine, and atypical ones, such as clozapine, modulate cytokines which are known to be produced by monocytes as well as by T helper (Th)1 and Th2 subpopulations.
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